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IHO > Week 4 > Flashcards

Week 4 Flashcards

0
Q

What do early pro B cells express? Intermediate? Late?

A

Early- TdT alone
Intermediate- both TdT and B220
Late- B220 and down regulated TdT

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1
Q

What 2 cytokines allow inflammatory cell recruitment?

A

IFN-gamma

TNF-alpha

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2
Q

What molecule modulates exchange for CLIP and antigenic peptide in MHC class 2 formation? What molecules blocks until acidic conditions?

A

HLA DM facilitates exchange

-HLA DO blocks DM (DO is only expressed in B cells and in thymus- helps DM only work in late endosome)

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3
Q

What enzyme is mutated in XLA immunodeficiency?

A

Bruton’s tyrosine kinase (Btk)

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4
Q

What ligand and receptors are mutated in Common Variable Immunodeficiency (CVID)?

A

CD40 ligand on T cells, B cell surface receptor CD19, activated T cell co-stimulatory molecules ICOS and TACI

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5
Q

Binding of what receptor on the T cell with B7 on APC is stimulatory? inactivating?

A
  • stimulatory= B7 with CD28

- inactivating= B7 with CTLA-4

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6
Q

What cells express MHC class 1? MHC class 2?

A
  • MHC class 1- most cells in body (except RBCs)

- MHC class 2- professional APCs (DCs, macrophages, B cells)

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7
Q

When do DCs, macrophages, B cells express MHC-class 2? (constantly, induced, etc)

A
  • DCs: constituitively express MHC-2 (also always express B7)
  • Macrophages: must be activated to express MHC class 2 and co-stimulatory molecules
  • B cells: constitutively express Class 2; must be activated to express co-stimulatory molecules
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8
Q

What MHC class is loaded by the cytosolic pathway?

A

-MHC class 1 (synthesized in RER; TAP1/2 to enter ER)

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9
Q

What MHC class is loaded by the endocytic pathway?

A

-MHC class 2

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10
Q

What is the normal ratio of CD4: CD8 T cells in the body?

A

~65% CD4 and ~35% CD8

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11
Q

What age does MHC class 1 deficiency affect patient? Susceptible to what infections?

A
  • young (age 4)

- susceptible viral infections: influenza, EBV

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12
Q

What age does MHC class 2 deficiency affect patient? (inherited autosomal recessive) Susceptible to what infections?

A
  • onset 6 months
  • mild form SCID (makes few T cells)
  • elevated WBCs (esp. neutrophils and lymphocytes)
  • low CD4+ T cells
  • no HLA-DQ or HLA-DR being formed
  • susceptible to pyogenic and opportunistic infections
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13
Q

How does classic SCID differ from milder form in case?

A
  • classic SCID: no T cells responding to any antigen

- milder form: T cells could be activated in vitro by PHA

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14
Q

Is there a treatment for MHC class 1 deficiency? Class 2?

A
  • MHC class 1 deficiency- no

- MHC class 2 deficiency- hematopoietic stem cell transplant

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15
Q

What cytokine induces expression of MHC class 2 molecules on APC?

A

Interferon- gamma

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16
Q

What are the cytokines required for B cell development?

A
  • IL-7: promotes B cell lineage development
  • Blys: survival of pre-immune B cells
  • IL4, IL3, L-BCGF: initiating B cell differentiation
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17
Q

Transitional immature B cells: Which receptor on surface for TI-1? TI-2? where do they help B cell go?

A
  • TI-1: transitional phase with IgM (T cell zone); negative selection
  • TI-2: transitional phase with IgM and IgD (go to follicle); positive selection
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18
Q

T-independent B cell activation: Which antigens are TI-1 antigens? TI-2?
-many TI antigens are PAMPs (recognized by TLRs)

A
  • TI-1: bacterial cell wall components; LPS (TLR4 or BCR)
  • TI-2: large polysaccharide molecules with repeating antigenic determinants (Ficoll, dextran, polymeric bact. flagellin, poliomyelitis virus)
  • activate B1 B cells
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19
Q

Which TLR causes nonspecific (polyclonal) activation?

Which receptor causes specific (clonal) activation?

A
  • TLR4= polyclonal
  • BCR= clonal
  • only IgM is produced
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20
Q

How do B1 B cells bind Type 2 TI antigen? What type of activation?

A
  • crosslinking BCR
  • specific (clonal) activation
  • mostly IgM produced
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21
Q

Expression of what CD molecule can identify B-1 cells?

A

-CD5

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22
Q

Where do B and T cells that recognize each other go? What does B cell need to express to survive?

A
  • go to germinal centers

- B cell must express Bcl-2 (to protect itself from apoptosis)

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23
Q

What does CD44 do in T cell development?

A

-CD44 is required for re-localization to the thymus

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24
Q

What stage in T cell development expresses CD44? CD25? CD3? CD4? CD8? CD117 (c-Kit)?

A
  • CD44- DN1 and DN2
  • CD25- DN2 and DN3
  • CD3- DN3 and beyond
  • CD4 and CD8- DP
  • CD4 or CD8- single positive
  • CD117 (c-Kit)- stem cell, lymphoid progenitor, DN1, DN2
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25
Q

Which polarizing cytokines induce Treg cells? master transcriptional regulator?

A
  • IL2, TGF-beta

- FOXP3

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26
Q

Which polarizing cytokines induce TH 17 cells? master transcriptional regulator?

A
  • IL1, IL6, IL23, TGF-beta

- ROR-gamma t

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27
Q

Which polarizing cytokines induce TH 2 cells? master transcriptional regulator?

A
  • IL4

- GATA3

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28
Q

Which polarizing cytokines induce T-FH cells? master transcriptional regulator?

A
  • IL6, IL21

- Bcl-6

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29
Q

Which polarizing cytokines induce TH-1 cells? master transcriptional regulator?

A
  • IL12, IFN-gamma, IL18

- T-Bet

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30
Q

What effector molecules are produced by CD8+ cytotoxic T cells? NK cells?
-how do the molecules work?

A
  • CD8+ CTLs: cytotoxins (perforins and granzymes), IFN-gamma, TNF, Fas ligand
  • NK cell: cytotoxins (perforins and granzymes), IFN-gamma, TNF, Fas ligand
  • both do cytotoxic granule release and FASL-FAS interactions
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31
Q

What cell surface proteins of CD4+ T cells and APCs are important in “licensing” APC for cross-presentation of antigen?

A
  • licensing of APC requires interaction with a CD4+ Th1 cell or direct interaction with a pathogen- TLR molecule
  • licensing of DCs occurs by: 1) CD40L + helper T cell, or 2) pathogen (via TLR)
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32
Q

Mechanisms of CTL killing:

A
  • Perforin (form pore) and granzyme(activate apoptosis by cleaving caspases) secretions
  • Fas ligand (cleave caspases)
  • TNF production and secretion
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33
Q

NK cells produce IFN-gamma- what effects does this have in cell production?

A
  • IFN-gamma tilts immune response toward Th1 by inhibiting Th2 cells and inducing IL-12 production by macrophages and DCs
  • IFN-gamma can activate M1 (angry) macrophages and NK cells
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34
Q

What 2 types of receptors can either activate or inhibit NK cells?

A
  • Lectin-like receptors (bind proteins rather than polysaccharides)
  • Immunoglobulin-like receptors (KIR= killer cell immunoglobulin-like receptors): bind to most MHC class 1 molecules
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35
Q

Which KIR family receptors work in inhibitory fashion? what ligands on potential target cells?

A
  • KIR2DL1: HLA-C2
  • KIR3DL1: HLA-Bw4
  • KIR3DL2: HLA-A3 and A111
  • KIR2DL2/3: HLA-C1

Only activating = KIR2DS1: HLA-C2

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36
Q

Which lectin-like family receptors work in inhibitory fashion? what are ligands they bind?

A

-CD94-NKG2A: HLA-E

all others are activating

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37
Q

What is the general process and cells involved with antibody-dependent cell mediated cytotoxicity (ADCC)?

A
  • Effector cells: NK, macrophages, monocytes, neutrophils, eosinophils
  • Effector cells bind antigen via Ab (through Fc receptor)
  • Killing: mediated by cytolytic enzyme release by macrophages, neutrophils, eosinophils
  • TNF release by NK cells, monocytes, macrophages
  • Perforin release by NK cells and eosinophils
  • Granzyme release by NK cells
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38
Q

What are the genetic abnormalities in Acute Promonocytic Leukemia (APML)?

A
  • inv(16); 11q23
  • treat promptly with hydroxyurea, leukopheresis, chemo
  • DIC with APML (M3)
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39
Q

With acute leukemia, what lab test should you run to test for choromosomal abnormalities?

A

-Cytogenetics

favorable risk= t(8;21), t(16;16); t(15;17); unfavorable risk= del5, del7, trisomy 8, 11q23

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40
Q

What new AML drug inhibits Flt-3 receptor tyrosine kinase?

A
  • Quizartinib

- notable SE: QTc prolongation (watch EKG)

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41
Q

What new AML drug targets CBF (core binding factor)?

A
  • Dasatinib

- c-Kit overexpression in CBF + AML

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42
Q

What diagnosis is characteristic of CD5+ CD23- cyclinD1+?

A

-Mantle cell lymphoma (aggressive NHL)

43
Q

What is the difference between CLL and SLL (small lymphocytic leukemia)?

A

-SLL is only in tissues (tissue phase of CLL)

44
Q

What are 2 poor prognostic factors of CLL? One good prognostic factor?

A
  • worse: CD38+ or ZAP-70+

- better prognosis: CD38-

45
Q

What drug causes loss of reflexes in 100% patients? (reflex loss is how drug dosage is determined enough)

A

-Vincristine (and Vinblastine?)

46
Q

Which plant alkaloid is not susceptible to MDR resistance?

A

-Ixabepilone

47
Q

What are the 2 immunosuppressive antibiotics used to prevent rejection after bone marrow transplants?

A

-Cyclosporine and Tacrolimus

48
Q

What target do Rituximab, Ibritumomab, and Tostitumomab bind? TU?

A
  • CD20

- B cell NHL

49
Q

What target does Gemtuzumab bind? TU?

A
  • CD33

- No longer used (removed from market?

50
Q

What target does Alemtuzumab bind? TU?

Specific toxicity?

A
  • CD52
  • B cell lymphocytic leukemia (B-CLL)
  • can cause cough and chest tightness
51
Q

What target does Denileukin-Diftitux bind? TU?

A
  • cells expressing IL-2R

- cutaneous T-cell lymphoma

52
Q

What cytokine can cause hand/foot syndrome, thrombocytopenia, shock, respiratory distress, fatal hypotension, and possible coma?

A

-Interleukin-2

53
Q

What cytokine decreases angiogenesis, decreases cell division, increased MHC-class 1 expression on tumor cells, and has possible SE of depression?

A
  • Interferon alpha

- other SEs: flu like Sx, hypotension, BMS

54
Q

Which cytokine has such a short half life it must be given IA, and has SEs of flu like Sx and possible hemorrhagic necrosis?

A

-Tumor necrosis factor- alpha

55
Q

Which hematopoietic agent increases production of neutrophils by stimulating G-CSF?

A

-Filgrastim

56
Q

Which hematopoietic agent increases production of granulocytes, eosinophils, basophils, and monocytes by stimulating GM-CSF?

A

-Sagramostim

57
Q

Which 2 hematopoietic agents increase platelet production?

A
  • Interleukin 11

- Thrombopoietin

58
Q

What do Dasatinib, Imatinib, and Nilotinib target?

A
  • Bcr-Abl

- treat CML

59
Q

What do Cetuximab, Erlotinib, Gefitinib, Lapatinib, and Panitumumab target?

A

-EGFR (a tyrosine kinase)

60
Q

What do Lapatinib and Trastuzumab target?

A
  • HER2 (a tyrosine kinase)
  • treat breast cancer
    toxicity: ventricular dysfunction/ CHF (ErbB2)
61
Q

What do Pazopanib, Sorafenib, and Sunitunib target?

A

PDGF-R and VEGF-R (angiogenesis)

62
Q

What is L-Asparaginase used to treat? Is MTX given before or after when used together?

A
  • childhood ALL

- must give MTX first to have synergy

63
Q

Which drug is competitive inhibitor of 26S proteosome? TU? Toxicities?

A
  • Bortezomib
  • used for multiple myeloma
  • Toxicity: thrombocytopenia, anemia, neutropenia, peripheral neuropathy
64
Q

Which drug is an HDAC inhibitor? Toxicities?

A
  • Vorinostat (suppression of suppression to cause apoptosis)

- Toxicity: PE, DVT, thrombocytopenia, anemia; interaction with Warfarin, N/V, diarrhea, hyperglycemia, dysgeusia

65
Q

What are the 3 differentiating agents? TU?

A

-Tretinoin
-Arsenic Trioxide (prolonged QT/ arrhythmias)
-Bexarotene (pancreatitis from hyperlipidemia)
Induce tumor cell differentiation leading to apoptosis
TU: Acute promyelocytic leukemia (APL)

66
Q

Which tyrosine kinase do Dasatinib, Imatinib, Nilotinib, and Sunitinib target? Cancer type?

A
  • c-kit
  • GIST (GI stromal tumors)
  • Dasatanib also targets Src (anti-metastatic in epithelial derived tumors)
67
Q

What is the mechanism of action for Erlotinib and Gefitinib?

A
  • competitive antagonists of ATP binding site of epithelial growth factor receptor (EGFR) tyrosine kinase
  • epithelial- derived cancers
68
Q

What are unique SE risks for Abl tyrosine blockers (Dasatinib, Imatinib, and Nilotinib)?

A
  • CHF and decreased left ventricular ejection fraction (causing shortness of breath, palpitations, fatigue) and/or MI
  • Abl tyrosine kinases are necessary for normal heart function
69
Q

What is a unique toxicity for Erlotinib and Gefitinib?

A

-interstitial pneumonia (which can be fatal)

70
Q

What do Everolimus and Temsirolimus block?

A

-mTOR

71
Q

What does Bevacizumab block?

A

-VEGF

72
Q

Which cytokine induces interferon-gamma which increases inducible protein 10? SE: GI and liver function effects (side effects decrease with time)

A

IL-12

-angiogenesis inhibition

73
Q

Which cytokine decreases cell division and increases MHC class 1 expression on cancer cells? Also decreases FGF production?

A
  • Interferon-alpha
  • depression is common side effect
  • anti-angiogenesis
74
Q

Which drug is anti-VEGF? Unique SEs: GI perforation, wound dehisence, hemoptysis?

A
  • Bevacizumab

- anti angiogenesis

75
Q

What do Pazopanib, Sorafinib, and Sunitinib do? Unique targets for each? TU?

A
  • all three target VEGF-R and PDGF-R
  • Sorafinib- also targets Raf
  • Pazo and Suni- also target c-kit
  • TU: renal cell carcinoma
76
Q

What are specific SEs unique to Pazopanib, Sorafinib, and Sunitunib?

A
  • Pazopanib: hepatotoxicity, hemorrage, GI performation, hypertension
  • Sorafinib: hemorrhage, hypertension
  • Sunitinib: hand-foot syndrome, skin discoloration
77
Q

What drug is used to treat Hansen’s disease, multiple myeloma, and off label use for AIDs? SE?

A
  • Thalidomide
  • N/V, rashes, peripheral neuropathy, increased risk DVT (treat with Warfarin right away)
  • severe birth defects (phocomelia- malformed intestines, hearing defects, ocular and retinal defects, deformed limbs)
78
Q

What is an example of recruitment (used to treat AML)?

A

-Daunorubicin and Cytarabine

79
Q

What are the 4 Chronic Myeloproliferative disorders? main cells in each?

A
  • CML- neutrophils
  • Polycythemia vera- red cells
  • Essential thrombocythemia- platelets
  • Myelofibrosis- everything
80
Q

Which chronic myeloproliferative disorder results from mutated Jak2 or too much EPO (secondary)?

A

Polycythemia Vera

81
Q

Which chronic myeloproliferative disorder can present with either bleeding or thrombosis?

A

Essential Thrombocythemia

82
Q

Which chronic myeloproliferative disorder has teardrop red cells?

A

Chronic Myelofibrosis

83
Q

What molecular event initiates CML?

A
  • translocation t(9;22)/ Philadelphia chromosome

- BCR-ABL fusion protein

84
Q

What are the activating changes in BCR-ABL1?

A
  • coiled-coil domain is added from BCR (promotes dimerization, necessary for activation)
  • Myristate attachment site lost from ABL1 (necessary for auto-inhibition of ABL1 TK activity)
  • Tyrosine-177 is added from BCR, phosphorylation creates new binding site for intracellular signaling proteins
85
Q

What does phosphorylation of Y177 on BCR fusion gene do? Why is it unique?

A
  • causes dysregulated proliferation and protection from apoptosis
  • BCR normal gene is not a TK (not P)
86
Q

In oncogenic signaling, BCR-ABL1 kinases activate what pathway in the cell?

A

-Jak2 to Stat5 (causes transcription of anti-apoptotic genes even when GM-CSF receptor not activated

87
Q

What disease is the TRAP stain positive for?

A

Hairy Cell leukemia

88
Q

What is the most common cause of lymphadenopathy? most common malignant cause?

A
  • most common a benign reaction to infection

- malignant: most likely metastatic carcinoma

89
Q

What type of macrophages are usually found in normal germinal centers?

A

Tingible body macrophages

90
Q

What cell markers are found in Small Lymphocytic Lymphoma (same as CLL)?

A
  • B cell lesion but also CD5+

- small mature lymphocytes

91
Q

What disease can be associated with Helicobacter pylori infections?

A
  • Malt lymphoma (type of Marginal Zone Lymphoma)

- give antibiotics

92
Q

What disease is associated with t(11;14)? (cyclinD and IgH translocation)

A

-Mantle Cell lymphoma

93
Q

What disease is associated with t(14;18)? (IgH and bcl-2)

A
  • Follicular lymphoma
  • “butt” cells
  • CD20 positive
94
Q

What disease is a T cell lymphoid process that has cerebriform lymphocytes, skin lesions, and blood involvement?
-can be mistaken for eczema or psoriasis

A

-Mycosis Fungoides/ Sezary Syndrome

95
Q

What disease is commonly a T-lyphoblastic lymphoma often in teenage male with mediastinal mass? (lymphoblasts in diffuse pattern)

A
  • Lymphoblastic Lymphoma
  • 2 types: B and T
  • same as ALL
96
Q

Which disease is associated with t(8;14) (c-myc and IgH)

A
  • Burkitt Lymphoma
  • starry-sky pattern
  • child with fast growing extranodal mass
97
Q

What disease has B-cell origin with popcorn cells?

A

Nodular L-P Hodgkin lymphoma

  • good prognosis (early stage)
  • asymptomatic young male with cervical lymphadenopathy
98
Q

Which drug is the most potent anti-TNF-alpha agent known?

-used to treat multiple myeloma

A

-Thalidomide

99
Q

What type of biopsy is needed for lymphoma diagnosis?

A

excisional biopsy

100
Q

What is the criteria for stagin lymphoma? Stage 1-4

A

Stage 1: single location
Stage 2: 2 or more locations; same side of diaphragm
Stage 3: both sides diaphragm
Stage 4: involving organs

101
Q

Which is the most common NHL in adults?

A

Diffuse large B cell Lymphoma (DLBCL)

-treated with CHOP

102
Q

Which drug specifically targets CD20?

A

Rituximab (really helped lymphoma treatments)

103
Q

What changes worsen and improve CLL prognosis?

A
  • worse: loss of TP53 (17p)

- favorable: 13q14.3 (13q)

104
Q

What drugs should you NOT give if you suspect lymphoma?

A

steroids (may shrink it before you know what it is) - need excisional biopsy

IHO (7 decks)

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